The Authie is a river in northern France whose 103-kilometre course crosses the departement of the Pas-de-Calais and the Somme. Its source is near the village of Coigneux, it flows through the towns of Doullens, Auxi-le-Château, Nempont-Saint-Firmin and Nampont flowing out into the Channel near Berck. Its regular course has attracted mankind for many centuries, developing an agricultural environment, still dominant today; the valley of the Authie, with many towns, villages and chateaux, holds a rich architectural heritage alongside the banks of the river, while the river mouth forms a sizeable bay between Fort-Mahon-Plage and Berck, typical of Picardy estuaries. The area is home to a diverse range of fauna; the origin of the name Authie has not been established with any certainty. A possibility is the pre-Celtic word atur meaning river, it was known in Latin as Alteia. Many waterways’ names, such as the Adour, are a corruption of the Celtic term alt meaning deep and that could refer to the steep-sided bed of the river.
Another suggestion stems from the Latin word attegia designating groups of fishermen and lumberjacks living by any river.. In the context of an oceanic/pluvial system, the Authie has a uniform and comparatively sustained outflow of 10.8 cubic metres per second at its outlet. The river flow is affected by the oceanic climate, characterized by an average annual temperature of 10 °C few days of frost, comparatively high rainfall between 800 and 900 mm per year except near the coast estuary where rainfall is less than 650 mm per year. Pas-de-Calais: Beauvoir-Wavans, Auxi-le-Château, Groffliers, Nempont-Saint-Firmin and Berck. Somme: Coigneux, Authieule, Hem-Hardinval, Dompierre-sur-Authie, Nampont and Fort-Mahon-Plage. Gérard Bacquet, Val d'Authie, Ed. Château, Auxi-le-Château, 1975 ASIN B0000DP6VS Eric Alibert, La Côte d'Opale, Carnet du Littoral, Gallimard - Conservatoire du littoral, 1998 ISBN 2-07-051467-6 Website of the Association for the development and promotion of the environment in the Val d'Authie.
Aascalys website dedicated to the rivers and countryside of Artois
Stuart Louis "Larry" Jacobus was a professional baseball pitcher from 1915 to 1927. He spent most of his career in the Texas League and played five games in Major League Baseball for the Cincinnati Reds. Jacobus weighed 186 pounds. Jacobus was born in Cincinnati, Ohio, in 1894, he started his professional baseball career in 1915 with the Ohio State League's Portsmouth Cobblers. That season, he helped Portsmouth win the pennant. Jacobus moved on to the Texas League's Galveston Pirates in 1916, he went 2-3 in his first year in 10-13 in his second. In September 1917, Jacobus was drafted by the Cincinnati Reds in the Rule 5 draft, he was with the team early in the following season but did not pitch well enough to appear in a regular season game until July. Jacobus made five relief appearances for the Reds in July and August 1918 and went 0-1 with a 5.71 earned run average. On August 13, he was released, the Pittsburgh Press reported that he " not in shape to work and of no use to the team."Jacobus spent the rest of his career in the Texas League.
He had winning records from 1919 to 1921. In 1921, he had his only 20-win season. In 1925, he went 9-22 to lead the league in that category, as well. Jacobus pitched for the Houston Buffaloes in 1926 and 1927. In February 1928, Jacobus was involved in a car accident, he lost the use of his right eye and never played professional baseball again. He died in at his home in North College Hill, Ohio, in 1965. Career statistics and player information from Baseball-Reference, or Baseball-Reference
Maresin 1 is a macrophage-derived mediator of inflammation resolution coined from macrophage mediator in resolving inflammation. Maresin 1, more defined maresins, are 12-lipoxygenase-derived metabolites of the omega-3 fatty acid, docosahexaenoic acid, that possess potent anti-inflammatory, pro-resolving and pro-healing properties similar to a variety of other members of the specialized proresolving mediators class of polyunsaturated fatty acid metabolites. SPM are dihydroxy and epoxy-hydroxy metabolites of long chain PUFA made by certain dioxygenase enzymes viz. cyclooxygenases and lipoxygenases. In addition to the maresins, this class of mediators includes: the 15-lipoxygenase -derived Lipoxin A4 and B4 metabolites of the omega 6 fatty acid, arachidonic acid. MaR1 was first defined as a product of DHA formed by cultures of human monocyte-derived macrophages. Studies implicate the following pathway in its formation: 12-lipoxygenase converts DHA to its 14-hydroxperoxy intermediate, 14-hydroperoxy-4Z,7Z,10Z,12E,16Z,19Z-DHA.
Byproducts of this metabolism include the reduction of 14-HpDHA to its hydroxyl counterpart, 14-hydroxy-4Z,7Z,10Z,12E,16Z,19Z-DHA. Concurrently, the macrophages convert DHA to 13,14-dihydroxy-4Z,7Z,9E,11E,16Z,19Z-docosapentaenoic acid, i.e. maresin 2. The measurement of 17-HDHA in tissues is used as a marker for the level of activation of the maresin-producing pathway; the maresins have been detected as products made by monocyte-macrophage cells types. MaR1 has been identified in the synovial fluid taken from the joins of patients with rheumatoid arthritis. In a murine model of acute respiratory distress syndrome, MaR1 production was detected. Planaria worms metabolize DHA to Mar1 during the healing phase of experimentally induced tissue injury. Studies suggest that maresins are involved in resolving inflammatory and allergic reactions, in wound healing, in abating neuropathic pain. Mar1 enhances the uptake of apoptotic human neutrophils by human macrophages, stimulates macrophage phagocytosis, limits the infiltration of neutrophils into the inflamed peritoneum of mice.
In a murine model of acute respiratory distress syndrome, MaR1 generation was detected in a temporally regulated manner with early MaR1 production was dependent on platelet-neutrophil interactions. In a murine model of a self-limiting pulmonary allergic reaction, MaR1 reduced lung inflammation, it appeared to act at least in part by augmenting the generation of regulatory T cells which interacted with Group 2 innate lymphoid cells to markedly suppress the production of two cytokines, Interleukin-5 and Interleukin-13, implicated in mediating allergic reactions. MaR1 accelerated tissue regeneration in experimentally injured planaria worms. In particular, it increasing the rate of head reappearance in beheaded worms. And, MaR1 reduced neuropathic pain in a mouse model by inhibiting a neuron ion channel, TRPV1, thereby blocking capsaicin-induced inward currents and neuron excitation. Mar2 possess at least some of the activities ascribed to MaR1, it enhances human macrophage phagocytosis of particles and efferocytosis of apoptotic human neutrophils and reduces neutrophil infiltration into the inflamed peritoneum of mice.
Its potencies ins producing these responses are similar to those of MaR1. 13,14-epoxy-maresin inhibits the production of the arachidonic acid metabolite, Leukotriene B4, by directly inactivating the enzyme, Leukotriene-A4 hydrolase, which converts the LTB4 precursor, Leukotriene A4, to LTB4. Studies find that the maresins inhibit certain pro-inflammatory functions in human neutrophils and macrophages in vitro, that MaR1 and Mar2 reduce the entry of blood neutrophils into the inflamed peritoneum in a mouse model, that Mar1 promotes the resolution of allergic pulmonary inflammation in a mouse model as well as wound healing in planaria worm model; these studies have not yet translated to human pathology. It is noted that MaR1 is detectable in the synovial fluid of patients with rheumatoi